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Citizenship Tangle
Anger in Assam as 2.5 lakh people included in draft citizens register face fresh hearings
Outfits like the All Assam Students' Union have raised objections to many names included in the draft NRC, forcing them to submit to time-consuming procedures.
Arunabh Saikia
The person who objected to Subrata Saha's inclusion in the National Register of Citizens draft list did not turn up at the hearing. | Arunabh Saikia
May 2 was supposed to be a hectic but happy day for Ashwini Kumar Saha, a resident of Bijni town in Assam's Chirang district. His younger daughter Abonti's prospective in-laws were in town to fix a date for the wedding.
Saha, who runs a bookstore, was happy about the match and had prepared well – there was a gift for each of the visitors who were coming from Nagaon, about six hours away by road. But at the last minute, he found they were one gift short. Determined to put up a good show, Saha rushed to his bookstore to collect some cash to buy a quick gift.
Waiting for him at the shop, however, was bad news. As he opened the shutters, he discovered a piece of paper slipped in under the door. It was a notice from the local office of the National Register of Citizens, asking him to appear for a hearing on May 7 along with the rest of his family. Someone called Sudip Chanda, the notice said, had objected to Saha's inclusion in the draft register, which aims to be a roster of bonafide Indian citizens in Assam.
Objections yet again
Of the 3.3 crore people who applied to be included in the National Register of Citizens, around 2.89 crore people have made it so far. To be included in the citizens list, an individual must prove that they or their ancestors entered the country before midnight on March 24, 1971. Those who did not make it to the draft list could make one last claim for inclusion before the final consolidated list is published, likely on July 31. Alongside this, objections could be filed against those included in the final draft.
The objection notice served to Saha implied that Chanda suspected he had migrated to Assam from Bangladesh after1971 and had been erroneously included in the draft list.
At first, Saha thought it was some elaborate prank. How could Chanda, the son of a man he grew up with, accuse him of being a foreigner? He hoped that the objection had been made by another person with the same name as his childhood friend's son. The notice, after all, mentioned no other details about Chanda except his name.
The next day, Saha's doubts were dispelled by Chanda himself. It was indeed his friend's son, a member of the local unit of the All Assam Students' Union, the outfit that has spearheaded anti-foreigner agitations in Assam.
"He came to me the next day and said, 'Sorry uncle, I have done a big mistake, I will withdraw the objection," Saha recalled. "You don't have to attend the hearing."'
To be safe, Saha presented himself at the hearing along with his family. His family was in town and the hearing centre was close by. "I went because it involved not just me, but everyone else in my family," he said. "If I am declared as a foreigner, so will my daughters. But at the hearing, the officer showed me a letter signed by Sudip [Chanda] saying that he had retracted his objection."
Ashwini Saha's objector withdrew the complaint.
Absent complainants
That was that. But Saha's experience was more an exception than the rule. Objections have been filed against more than 2.5 lakh people who are on the draft list, mostly by the state's powerful sub-nationalist outfits, such as the All Assam Students' Union.
Unlike Saha, most cannot know beforehand who the complainant is and why they have raised objections. The notice only mentions the objector's name.
They have little choice but to turn up at the hearing with their extended families, many of whom travel formidable distances to testify in favour of their targetted relative.
On the other hand, hardly any of the complainants have attended the hearings since they began on May 6, according to officials involved in the exercise. In the absence of the objector, the rules say, the complaint should be disposed off ex parte. But that is not how it works on the ground.
'Self-contradicting'
Take the example of Bongaingaon's Mokibul Islam, who appeared for his hearing on May 15 in Barpeta town. A person named Jyotishman Das had objected to his inclusion in the draft register.
Islam, who works in a plastic factory in Guwahati, did not just have to travel all the way to Barpeta, 96 km away from Guwahati, for his hearing but also had to bring 13 of his relatives from different parts of Bongaigaon and Barpeta. They had all received summons from authorities to be present at the hearing.
Although the objector, Das, failed to turn up, the National Register of Citizens official entrusted to deal with the case asked for Islam's "legacy data code", an 11-digit number attached to the person applicants trace their ancestry to. In Islam's case, it is his grandfather, Simijuddin, who features in the 1966 electoral rolls.
After rummaging through his polythene bag full of documents, Islam told the official that he had forgotten to get the print-out bearing the legacy code. But he had got along everything else, he insisted. A copy of the 1966 electoral rolls with Simijuddin's name, voter ID cards – his father's and grandfather's in addition to his own – to prove that he was indeed Mokibul Islam, son of Kismat Ali, grandson of Simijuddin, permanent resident of Goroimari village, Bijni circle, Bongaingaon district. Besides, Simijuddin himself was present there too.
Kismat Ali and his father, Simijuddin. Simijuddin's name features in the 1966 electoral rolls -- a fact verified by the National Register of Citizens authorities after multiple checks.
The official refused to budge, forcing Islam to make the 55-km journey back to the family's ancestral home in Goroimari village to get the document. As the rest of the family stayed put at the makeshift hearing centre, tempers frayed, with everyone blaming each other for the lapse.
The rising mercury and an empty Ramzan stomach made Kismat Ali particularly cantankerous. When a concerned relative asked him to calm down, he shot back: "How can I not worry? It is a matter of my son's citizenship."
Why should people who have been included in the draft register after a long-drawn, rigorous process be asked to produce anything at all when the complainant herself is absent, activists ask. The rules also say as much: "In case of absence of objector, hearing to be disposed ex-parte".
National Register of Citizens officials at the local level say they check because they have been given verbal orders to do so. But the concede that it is a "self-contradicting exercise". "It is unnecessary harassment that everyone, the people, the officials, could have done without," said a disposal officer appointed to examine objections.
No written acknowledgement
Even after officials disposed off objections ex parte, the rules prevent them from providing anything in writing to members of the public. The official notes down "objector absent" in his records but no copy of it is given to the objectee. Taking photographs is also prohibited.
"This violates all bureaucratic rules," complained Firdoush Ali, who works as a supervisor at a construction company in Guwahati.
The person who objected to his inclusion in the draft list failed to turn up at the hearing held in Barpeta, leading to the complaint being disposed off. But Ali has no paperwork to prove that. "There is simply no acknowledgement that we were here," he said. "I came from Guwahati; my cousins have come from Goalpara and Dhubri. Tomorrow if they say we were not here, I have literally nothing to prove otherwise."
Taking biometric data
People whose inclusion in the draft list has been objected to are resentful that complainants can fail to turn up at the hearing without facing any penalty – and their identity is withheld too.
According to the standard operating procedure, there is no penalty against the complainant if their objection is found to be invalid. However, the rules state that "knowingly" submitting false representations is a crime under India's citizenship law, which is applicable for people making claims as well as objections.
"My objector did not turn up, so what did they do?" said an indignant Subrata Saha whose hearing took place on May 7. "They took my biometrics like I am some thief who will run away in spite of me telling them that I already have an Aadhaar card."
It was only on May 11 that the National Register of Citizens state coordinator Prateek Hajela passed an order calling for cases to be disposed off ex-parte in the absence of the objector.
Subrata Saha said that he had written to the local district administration to delete his biometric details since his name features in the draft list.
The Assam government has collaborated with the Unique Identification Authority of India, which runs Aadhaar, to collect the biometric data of people who were left out of the draft list and have filed fresh claims to be included.
"I am not letting it go, if they don't listen, I will write to Hajela," he affirmed. "Also, I am not letting go without finding out who has filed an objection against me. If need be, I will file an RTI [a petition under the Right to Information Act]."
What explains the fact that most people who have received objection notices claim to not know their complainants at all in most cases? In the absence of any connections between the objector and objectee, why were some singled out and not others? After all, logic dictates that someone would object to the inclusion of another person in the register only if they had reason to believe that they were recent migrants.
Conversations with local All Assam Students' Union leaders made things clearer.
A woman waiting to submit her biometric details at an National Register of Citizens office in Barpeta.
Mass objections
Amarendra Mishra, the president of the Barpeta district unit of the All Assam Students' Union, claimed to have filed around 150 objections. That was when he was the president of the group's unit in Sarbhog, a town in Barpeta. Mishra conceded that he did not know almost any of the 150 people whose inclusion he had contested.
"I received ARN numbers from our district office and I filed objections against them," said Mishra.
The ARN, or application receipt number, is a 21-digit number linked to each application. Although not publicly available, all local National Register of Citizens offices, circle and deputy commissioners' offices maintain with them an area-wise list of all applicants and their corresponding application numbers.
Mishra claimed that he was told by his district colleagues that most of the application numbers he was supplied with were of people living in Barpeta's char areas. Chars are shifting riverine islands on the Brahmaputra populated largely by Bengali Muslims.
Chanda, who filed the objection against Ashwini Saha , seconded Mishra's claim about receiving a list of application receipt numbers from the district headquarters of his organisation. "We then divided the work among ourselves," he said. "I personally did some 150."
On what basis were the application numbers selected?
"The Supreme Court has given us the right to file objections, so we have collected as many ARNs [Application Receipt Numbers] as possible," explained Deepak Kumar Das, a colleague of Chanda's who claimed to have filed around 200 objections. "It is the responsibility of the NRC [National Register of Citizens] authorities to examine them now. We should have done more, but we could not collect more ARNs."
People waiting for their hearing at a makeshift National Register of Citizens centre in Barpeta.
'Collateral damage'
Both Das and Chanda admitted that they had no idea whom they were filing objections against, which explains the objection notice Ashwini Saha received with Chanda as the complainant.
"AASU [All Assam Students' Union] is a party to the NRC [National Register of Citizens] case in the Supreme Court as you may know," said Das. "So, it was decided by our advisers and central committee that we should do something for an error-free NRC. We are a hierarchical organisation, the orders were then given to the district committees to follow who then gave us a list of ARNs [Application Receipt Numbers]."
Chanda conceded that "not all objections we have filed pertain to illegal Bangladeshis". "We had to do it in a hurry, sometimes my hand could have slipped and I may have written a few wrong digits," he said. "After all, it is an 11-digit number and we had to do so many in such a short time."
But they insist that there is no other way to other way to prevent "illegal Bangladeshis" from creeping into the National Register of Citizens.
"We are doing it for the Assamese people," Das said. "If you do some good work, there will be collateral damage. It should be taken positively. If out of the 2 lakh objections, even 20,000 people are really guilty, we will consider it as an achievement. If not for us, these people would have been naturalised as legal citizens."
Chanda agreed. He did not understand what the fuss was about.
"What is the problem? Why can't they [people at the receiving end of these objections] just go," he asked. "Can't they do that much to be in the NRC [National Register of Citizens]?"
But what has prevented the objectors from attending the hearings?
The answers vary. Mishra said he did not receive any summons. "I did receive a call from the block, but there was no notice to be present," he claimed. "So, I have not gone yet."
Chanda blamed it on the schedule of hearings. "I have filed 150 objections," he said. "The hearing dates have clashed. In one day, there are 20 hearings, all in different places, how can I be there everywhere?"
Das also offered a similar explanation. "If they were to happen in a convenient place and time, I would attend it," he said. "But anyway, we have done our job, it is now for the NRC [National Register of Citizens] officials to investigate the complaint."
When leaders of the Assamese students' outfit are told that minority groups such as the Assam State Jamiat Ulama and the All Assam Minority Students' Union have alleged that several "fake" objections have been filed to harass a particular community, they point at the rule book.
"We are not saying that the people we have filed objections against are Bangladeshis for sure, we have only acted out of suspicion – and the rules let us do that," contended Mishra. "It is a complete lie that we have acted on communal lines."
Anita Sarkar and her husband Prabir Sarkar. Anita Sarkar's brother took the train from Bengal to attend her hearing but the objector failed to turn up.
'Is the AASU office a court?'
People at the receiving end of these objections, however, say that such complaints amount to vigilantism.
"I told the NRC [National Register of Citizens] officials that I do not value their word anymore because they have already verified my documents, not once but several times," said Subrata Saha. "So, I told them, call the complainant and let him certify them [the documents] since it is clearly their word that matters more than the system."
Prabir Sarkar, whose wife Anita Sarkar's inclusion was contested by Chanda, was equally scathing. Anita Sarkar hails from Bengal and her brother had to come down from the neighbouring state to Chirang as a witness for her hearing. Chanda failed to turn up yet again.
"I went to the centre three times but no one came," he said. "There someone told me I should go to the AASU [All Assam Students' Union] office and get it in writing from them that it is a mistake. I refused flatly. Are they judges now? Is the AASU office the new court?"
All photographs by Arunabh Saikia.
Corrections and clarifications: An earlier version of the story said that in absence of the objector, rules say that the complaint should be "dismissed" ex parte. However, the rules say that the case should be "disposed" ex parte.
NRC draft list
NRC final draft
NRC objections
Kafeel Khan case: SC rejects UP appeal against quashing of doctor's detention under NSA


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Guinea: Ebola, the Executive Summary – October 8, 2015
by Anthony Bee-ContehPosted on October 10, 2015
To give you deeper insight into what's happening in the Ebola outbreak, we've organized the latest developments in a curated weekly summary
West Africa Marks the First Week Without New Ebola Cases
For the first time since West Africa's Ebola outbreak began, the world has marked the first week without any new recorded cases.
According to data released on Wednesday by the World Health Organization (WHO), zero cases were recorded in the week leading up to October 4.
"This is the first time that a complete epidemiological week has elapsed with zero confirmed cases since March 2014," the WHO said in its latest situation report.
It added that all contacts have completed follow-up in Sierra Leone; no cases were recorded there in the past 3 weeks, meaning that the country is now more than halfway through the WHO's stipulated 42-day period before being declared free of Ebola.
But as the BBC points out, several high-risk contacts linked to recent patients in Guinea and Sierra Leone are missing from follow-up. In Guinea, over 500 contacts remain on the contact list and 11 patients remain in Ebola treatment centers, according to the latest Inter-Agency Collaboration on Ebola report.
Study: Sharp Rise in Maternal and Infant Mortality During Sierra Leone's Ebola Outbreak
The number of women dying during or after childbirth rose by 30 percent between May 2014 and April 2015 in Sierra Leone, according to a study by the Liverpool School of Tropical Medicine in partnership with VSO International.
The study also found that neonatal deaths rose by almost a quarter compared to the previous year. There was an 18 percent decrease in women accessing antenatal care, it said, drawing on research from 76 health facilities around the country.
Sierra Leone already had one of the worst maternal and infant mortality rates in the world before the outbreak struck, further denting public confidence in the weak health system.
The study recommends "the implementation of nationwide, long-term health education programs to inform the public about vital antenatal and post-natal care visits and assisted childbirth as well as taking measures to increase public confidence by improving the capacity of health care facilities and better provision of safe, quality services."
According to Peter Nderitu, VSO's Sierra Leone country director, "this research shows that Sierra Leone's health care system was still able to provide basic patient care throughout the Ebola crisis, but the real challenge was lack of public confidence in the safety of those services during that difficult time. Rebuilding public trust in health services is critical to improving maternal and newborn health."
As Cases Fall, Stigma Still Lingers in Some Communities
The outbreak may be closer than ever to ending, but for Ebola survivors and those who lost relatives to the virus, stigma remains high.
As IRIN Africa reports, some Ebola orphans in Liberia still suffer from bullying and social exclusion. One 14-year-old boy told IRIN that he is dubbed the "Ebola orphan" and is left out of meals with former friends. "This makes me sad," he said. "Many times they shun me and call me names." Another orphan, aged 16, told IRIN that her relatives refuse to spend time with her, still fearing that she might spread the virus.
Fatou Wurie, a Sierra Leonean activist and the co-founder of the Survivor Dream Project, writes in the Huffington Post that mixed public messaging around the dangers of sexual transmission of Ebola has left many people confused.
"For the public, the message is not clear," Wurie writes. "To accept survivors or to be cautious around survivors. Without clear scientific guiding evidence, the onus lies disproportionately on survivors to get it right at being safe and that is a heavy burden which the WHO alludes to as the 'emergency within the emergency.'"
A three-day survivors' workshop in Kindia, Guinea, ended on Wednesday, also partly designed to address stigma. Guinea has 1,261 registered survivors of Ebola.
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With 2.5 billion smartphones in the world today, some 50 microprocessors in your car, and countless chips connecting all of our appliances, the silicon semiconductor market just keeps expanding. With 20% year-on-year growth in 2018, the chip market came close to a record $500 billion in revenue. And for each new chip generation, demand for hydrogen peroxide (H2O2) goes up exponentially, including for Solvay's ultra-high-purity Interox® PicoPlus H2O2 for semiconductors.
INTEROX® Pico and PicoPlus are part of a range of chemicals produced by Solvay's GBU Special Chem and used primarily in the cleaning and etching stages of semiconductor chip production. Solvay is one of only a few companies in the world able to meet the exacting requirements of the leading semiconductor manufacturers.
To understand the level of product purity demanded by the chipmakers, picture a grain of salt in an Olympic-size swimming pool. That is a single digit part per trillion (ppt), which is the level of purity that Solvay's INTEROX® PicoPlus Hydrogen Peroxide needs to comply with for the electronics industry.
This is because chipmakers are working at a scale that is almost beyond imagination. The latest generation circuits are mere nanometers, so the purity of the product is paramount. They must avoid any contamination, since even a tiny particle can be a major threat to the workings of a nano-size chip.
The highest possible product purity is not enough, however. The semiconductor industry also requires consistency and reliability from Solvay as a supplier. They need Solvay to exert end-to-end process control and quality management along the entire value chain. This means not only Solvay's own processes, but also those of its suppliers and sub-suppliers.
On top of that, chipmakers also need security of supply. A 'fab,' as a semiconductor chip plant is called, costs some $10 billion to build, so manufacturers are under immense pressure to maintain production levels in order to amortize costs. Holding up the fabrication process because a supplier fails to meet customer requirements would cost millions per day.
As the largest H2O2 supplier in the world, Solvay is able to safeguard supply with its network of 16 hydrogen peroxide manufacturing plants globally, including in Germany, Italy, the United States, Thailand and, most recently, in China. This worldwide presence ensures Solvay stays close to its customers, providing immediate support and security of supply.


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Chapter 105. Cutaneous Manifestations of Drug Abuse
Haley Naik; Richard Allen Johnson
Naik H, Johnson R. Naik H, & Johnson R Naik, Haley, and Richard Allen Johnson.Chapter 105. Cutaneous Manifestations of Drug Abuse. In: Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K. Goldsmith L.A., & Katz S.I., & Gilchrest B.A., & Paller A.S., & Leffell D.J., & Wolff K(Eds.),Eds. Lowell A. Goldsmith, et al.eds. Fitzpatrick's Dermatology in General Medicine, 8e. McGraw Hill; 2012. Accessed January 30, 2023. https://accessmedicine.mhmedical.com/content.aspx?bookid=392&sectionid=41138817
Naik H, Johnson R. Naik H, & Johnson R Naik, Haley, and Richard Allen Johnson. (2012). Chapter 105. cutaneous manifestations of drug abuse. Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K. Goldsmith L.A., & Katz S.I., & Gilchrest B.A., & Paller A.S., & Leffell D.J., & Wolff K(Eds.),Eds. Lowell A. Goldsmith, et al. Fitzpatrick's Dermatology in General Medicine, 8e. McGraw Hill. https://accessmedicine.mhmedical.com/content.aspx?bookid=392&sectionid=41138817
Naik H, Johnson R. Naik H, & Johnson R Naik, Haley, and Richard Allen Johnson. "Chapter 105. Cutaneous Manifestations of Drug Abuse." Fitzpatrick's Dermatology in General Medicine, 8e Goldsmith LA, Katz SI, Gilchrest BA, Paller AS, Leffell DJ, Wolff K. Goldsmith L.A., & Katz S.I., & Gilchrest B.A., & Paller A.S., & Leffell D.J., & Wolff K(Eds.),Eds. Lowell A. Goldsmith, et al. McGraw Hill, 2012, https://accessmedicine.mhmedical.com/content.aspx?bookid=392&sectionid=41138817.
Cutaneous Manifestations of Drug Abuse: Introduction
Clinical Findings Associated with Commonly Used Drugs
Mucocutaneous Manifestations of Drug Abuse at a Glance
The morphology and arrangement of skin lesions can identify persons with former and current drug dependency.
Skin lesions associated with drug use can be related directly to the drug itself, mode of drug delivery, and/or adulterants or infectious agents mixed with the drug.
Drug addiction-related bacterial infections predominantly involve the skin and soft tissue. Culture-guided antibiotic therapy is essential because infection with unusual organisms, antibiotic-resistant strains, and polymicrobes is more common.
Behavioral effects of drug use can lead to the transmission of sexually transmitted diseases and blood-borne pathogens including Treponema pallidum, hepatitis B virus, hepatitis C virus, human immunodeficiency virus, and human T-lymphotropic viruses 1 and 2.
Drug abuse and addiction can be suspected or diagnosed on the basis of mucosal and cutaneous findings. The administration of drugs may cause cutaneous stigmata and eruptions predominantly through local or systemic, toxic or hypersensitivity-induced effects as a result of the drug itself, adulterants, infectious agents, or the mode of drug delivery.
Illicit drug use is a maladaptive pattern involving self-administration of prescribed or recreational drugs. Chipping is a lay term used to describe a pattern of drug use in which the user is not physically dependent, but rather sustains "controlled use" of a drug. A certain percentage of users will progress to drug dependence, a physical and/or psychological need for the effects of a chemical in order to avoid withdrawal symptoms associated with abstinence (Box 105-1). Drug dependence often leads to drug abuse, an intense desire to recurrently obtain increasing amounts of one or more chemical substances to the exclusion of all other activities, resulting in clinically significant physical, emotional or social distress (Box 105-2). Tolerance defines a physiologic state in which progressive increases in the dose of a drug are needed to achieve the effects previously experienced at smaller doses. Some drugs chiefly induce physical dependence, while cause predominantly psychological dependence.1
Box 105-1 Criteria for Drug Dependence
The presence of three or more of the following, occurring any time in the same 12-month period:
Withdrawal symptoms
Sustained intent or unsuccessful efforts to abate drug use
Administration of drug in higher doses and longer duration than initially intended
Significant time devoted to obtaining the drug or recovering from its effects
Relinquishment or reduction of social, occupational or recreational activities because of drug abuse
Continued drug use despite awareness of the presence of a persistent or recurrent physical or psychological problem caused or exacerbated by the drug
Adapted from American Psychiatric Association: Diagnostic and Statistical Manual of Mental Disorders IV-TR, 4th edition. Washington DC, American Psychiatric Press, 2000.
Box 105-2 Criteria for Drug Abuse
The presence of one or more of the following, occurring within a 12-month period:
Recurrent substance use resulting in a failure to fulfill major role obligations at work school, or home
Recurrent substance use in physically hazardous situations
Recurrent substance-related legal problems
Continued substance use despite having persistent or recurrent substance-related social or interpersonal problems
The National Institute of Drug Abuse (NIDA) (http://www.drugabuse.gov/)2 considers the following agents to be drugs of abuse in the United States:
Lysergic acid diethylamide (LSD)
3,4-Methylenedioxymethamphetamine (MDMA, Ecstasy)
Phencyclidine (PCP)
Steroids (anabolic)
Betel is widely used in South Asia, Southeast Asia and the South Pacific.
In 2004, the United Nations' World Drug Report estimated that between 3% and 5% of the global population used illicit drugs.3 In 2008, the National Survey on Drug Use and Health in the United States estimated that:
20.1 million Americans aged 12 or older (8% of that population) were currently using illicit drugs including marijuana/hashish, cocaine, crack, heroin, hallucinogens, inhalants or prescription-type psychotherapeutics.
Marijuana was the most commonly used illicit drug (15.2 million past month users).
The most commonly injected drugs were heroin and cocaine.
Almost 2 million current cocaine users, comprising 0.7% of the population, were estimated.4
The actual number of individuals who use heroin is difficult to determine because there has been a growing tendency to sniff, snort or smoke rather than to inject heroin intravenously or subcutaneously.
An estimated 70.9 million Americans (28.4%) aged 12 or older were current users of tobacco in any form.
Of Americans aged 12 and older, 51.6% had consumed alcohol at least once in the 30 days prior to being surveyed; 23.3% reported drinking heavily (>5 drinks on >5 occasions).
The drugs most commonly associated with emergency department visits in 2001 included cocaine, marijuana, benzodiazepines and heroin, in that order (Fig. 105-1).
Number of emergency department visits associated with various drugs. Cocaine, marijuana and benzodiazepines were the most common drugs associated with emergency department visits in 2001. Data from the United States Substance Abuse and Mental Health Services Administration, 2001, http://thedea.org/statistics.html.158
Studies in concordant twins have shown a strong influence of genetic inheritance on the susceptibility to drug use.5 The potential of a drug to cause addiction varies. The processes by which genes regulate physical reactions to addictive drugs have not been clearly elucidated. Repeated exposure to cocaine causes a change at the level of gene expression that leads to altered levels of the specific brain protein called cyclin-dependent kinase-5. This protein regulates the action of dopamine, which potentiates the euphoric effects of cocaine and other drugs.6 Narcotics disable the neurons that normally inhibit the release of dopamine while amphetamines and cocaine increase dopamine signaling, either by directly stimulating its release, or by blocking its absorption. Environmental factors such as history of sexual abuse during childhood, severe family dysfunction with drug abusing, detached or mentally ill parents, poor social skills, and drug-using peers are also clearly important.
The mechanisms of addiction, tolerance and dependence are complex. Addictive drugs flood the synapses of the mesolimbic system, especially the nucleus accumbens, with excessive amounts of dopamine, augmenting the hedonic tone and producing a euphoric state. The subsequent pleasurable reactions of the frontal cortex, amygdala, and hippocampus are exaggerated. The association of drug use and euphoria in these brain areas is reinforced with each exposure until the user no longer controls behavior, at which point addiction has resulted.7 Chronic users have sustained activation of the cAMP response element-binding (CREB) protein, a trigger for the production of dynorphin and other proteins that shut off dopamine release, preventing the individual from finding pleasure in usually enjoyable activities and requiring subsequent fixes with higher doses of drug to overcome the effects of tolerance. Addictive drugs also inhibit or excite neuronal activity in various areas of the nervous system. To compensate for these alterations, neuroadaptation develops with either formation of new neuroreceptor sites or diminished synthesis and sensitivity of neurotransmitters and neuroreceptor sites. Discontinuation of the drug reverses the neuroadaptation process and results in an exaggerated neural response that produces withdrawal symptoms.
Ethyl alcohol, or ethanol, is the intoxicating ingredient found in alcoholic beverages. It is a central nervous system depressant that impairs brain function and motor skills and is rapidly absorbed from the stomach and small intestine into the bloodstream. Heavy use can increase the risk of liver disease, stroke and certain cancers.
Direct liver toxicity of alcohol can cause hepatomegaly, jaundice, shrunken liver in the setting of cirrhosis, and hypoalbuminemia leading to Muehrcke lines and Terry nails (see Chapter 89). Hyperestrogenemia can lead to gynecomastia, palmar erythema, spider angiomata, and testicular atrophy. Portal hypertension secondary to alcohol-induced liver cirrhosis can lead to an enlarged spleen, ascites, variceal bleeding, hemorrhoidal bleeding and caput medusae. Dupuytren contractures due to fibroblastic proliferation and disorderly collagen deposition may be seen in 66% of alcohol abusers. Asterixis and confusion are seen in patients with hepatic encephalopathy. Alcohol withdrawal delirium, also known as delirium tremens, is characterized by tachycardia, hypertension, body temperature elevation and delirium. Ataxia, confusion and lateral gaze palsy are indications of Wernicke encephalopathy. Wernicke encephalopathy followed by anterograde and retrograde amnesia along with confabulation characterize Korsakoff syndrome.
Club drugs include γ-hydroxybutyric acid (GHB, date rape drug), flunitrazepam (Rohypnol®, roofies), ketamine, MDMA, and LSD (Table 105-1). These drugs tend to be used by teenagers and young adults in social settings. In 2008, NIDA showed that among 12th graders, 1.3% had abused flunitrazepam, 1.2% had abused GHB and 1.5% had abused ketamine at least once in the year prior to their being surveyed.8 GHB is sedating and can cause coma and seizures. It is being used increasingly by bodybuilders, who believe that it helps to metabolize fat and build muscle. Flunitrazepam is also sedating and can incapacitate users and cause amnesia; when combined with alcohol, this drug can be lethal. Ketamine distorts perception and produces feelings of detachment from the environment and self.
Table 105-1 Drugs: Street Names and Routes of Administration
Street Namesa
Route of Administration
Gym candy
Bunga (Tagalog)
Cau (Vietnamese)
Jambe (Javanese)
Kunya (Burmese)
Paan (Sanskrit)
Supadi (Nepali)
Shupari (Bengali)
Chewed
Bogie, cancer stick, cigs (cigarettes)
Chaw, snuff, chew (smokeless tobacco)
Smoke inhalation
Georgia Home Boy
Liquid ecstasy
Flunitrazepam
Roofies
Special K
Nasal inhalation
Transdermal application
Wack
Prescription medications: Opioids, CNS depressants, stimulants
Dust, dillies (dilaudid)
Emsel, God's drug (morphine)
Oxy, cotton (oxycontin)
Rids, vitamin R (Ritalin)
aMore terms at NIDA (National Institute of Drug Abuse) http://www.drugabuse.gov and Office of National Drug Control Policy website http://www.whitehousedrugpolicy.gov.2,159
Cocaine (benzoylmethylecgonine) is an alkaloid extracted from the leaves of the coca plant Erythroxylon coca.9–15 It is a powerful sympathomimetic, vasoconstrictor, local anesthetic, and stimulant. Cocaine hydrochloride is a powder that can be can be nasally inhaled or injected intravenously or subcutaneously, also known as "skin popping" (Fig. 105-2). Crack cocaine or "crack," the freebase rock crystal form of cocaine hydrochloride, is smoked (Table 105-1). Freebase refers to the pure basic form of an amine, as opposed to its salt form. The amine is usually a natural alkaloid product.
Skin popping scars. Multiple white angular atrophic scars on the dorsal forearms and hands.
Cocaine can produce intense vasoconstrictive effects by directly stimulating the central nervous system and increasing peripheral catecholamines. The vasospastic action of cocaine is greatest at one hour after use and can be associated with ischemia, infarction and hemorrhagic injuries of most organ systems including the skin.16–18 The ischemic effects of cocaine in the skin can lead to acute multifocal skin necrosis,19 chronic skin ulcers,20 cutaneous fibrosis,21 blackened hyperkeratotic "crack hands"22 and claw-like "parrot beak" curvature of the nails. These changes are commonly found in association with pernio and some atrophy of the distal portions of the digital pulp secondary to ischemia. At skin-popping sites, there may be central pallor surrounded by ecchymosis due to the vasoconstrictive properties of cocaine acting locally at the injection site with hemorrhage occurring in the surrounding tissue. Skin popping is a method of drug administration whereby a substance is injected subcutaneously or intradermally, but not intravenously and not typically intramuscularly. Individuals with vasomotor instability are more susceptible to these types of reactions.23
Inadvertent or deliberate direct intraarterial injection of cocaine can cause severe tissue ischemia and necrosis via direct vasoconstriction. Individuals experience an initial intense burning pain, followed by cyanosis and marked edema. Compartment syndrome may also result. In the most severe cases necrosis leads to amputation.24,25 Skin popping also puts one at risk for developing secondary amyloidosis.
Cocaine-induced vasospasm may cause major internal organ injury including acute myocardial ischemia, cerebrovascular accidents, renal infarction26 and splenic infarction.18,27 Vasoconstriction of mesenteric vessels and the direct toxic effect of cocaine on gastrointestinal mucosa can result in acute abdominal crises (known as crack belly) secondary to perforations, intestinal ischemia and infarction.28,29
Various vasculitic and vasculopathic processes have been associated with cocaine use including pseudovasculitis,30 urticarial vasculitis,31 Churg–Strauss vasculitis,32 Raynaud phenomenon,33,34 Henoch–Schonlein purpura, necrotizing vasculitis35,36 and Buerger disease (see Chapters 163, 164, and 173).37,38
The local anesthetic properties of cocaine make it difficult for individuals to feel traumatic injury. This leaves users prone to repetitive trauma from the irritant properties of the drug itself and implements of drug delivery, thus exposing them to an increased risk of infection.39 Missing a vein and injecting into the surrounding tissue creates a niche environment in which bacteria can thrive.40 Repeated needlesticks increase the likelihood of cutaneous infection and transmission of blood-borne viruses.41
Mucosal manifestations of ischemia secondary to cocaine inhalation or smoking include dental caries,42 gingival recession,43 oral blisters44 and nasal and palatal perforation.45 Insufflating (snorting) cocaine may lead to recurrent epistaxis, intranasal crusting, rhinitis and chronic sinusitis.42,46 Inhalation utensils themselves can act as vectors for viruses and may induce "snorter's warts." Nasal septum perforation reduces nasal support and results in a broad, flat nose or "saddle nose deformity."46–49 Nasal septum perforation typically occurs prior to development of palatal perforation. Cocaine burns of the upper airway are associated with hoarseness, dysphonia, odynophagia, dysphagia and stridor.23,26,50–53 Crack cocaine smoke has a direct toxic effect on the corneal epithelium of the eye. Repeated exposure to the alkaloid smoke may cause an irritant effect leading to excessive eye rubbing and subsequent infectious complications, and chemical burns.51
Drug reactions including acute generalized exanthematous pustulosis54 and Stevens–Johnson syndrome 55 have also been reported.
The stimulant properties of cocaine are associated with increased metabolism and dramatic weight loss.56 Psychiatric conditions, most commonly delusions of parasitosis and subsequent formication are experienced approximately 20% of the time in cocaine users (also known as coke bugs)57 (see Chapter 104). Recent reports have emerged of febrile agranulocytosis and often vasculitis with prominent involvement of the ear lobes secondary to cocaine adulterated with levamisole, an anthelmintic medication used in veterinary medicine to control parasites in livestock.58,59
Natural and semisynthetic derivatives of the opium poppy are known as opiates. Biologically natural opiates include morphine and codeine, while semisynthetic opiates such as heroin and hydromorphone are derived from biologically active opiates. Diacetylmorphine, or heroin, crosses the blood–brain barrier and binds opioid receptors in the brain, resulting in its euphoric, analgesic and anxiolytic effects. Heroin is the most common parenterally injected illicit drug, either by intravenous or subcutaneous (skin popping) administration. Heroin may also be inhaled. With a peak "rush" at 7–8 seconds, it is the fastest-acting and via smoking most potent opiate, accounting for up to 90% of opiate use in the United States.
Scarring is the primary cutaneous stigma of injection drug use. The antecubital fossa is the usual starting point of intravenous drug use, followed sequentially by the upper arms, hands, neck, feet, legs, groin and digits.60 Linear cord-like scars along a vascular distribution (track-marks), are formed after repeated injections along a superficial vein, resulting in venous thrombosis and subsequent fibrosis.61 (Fig. 105-3) Skin popping scars are irregular round hypopigmented or hyperpigmented, atrophic or hypertrophic scars or keloids.62 (see Fig. 105-2) Soot tattoos or shooting tattoos result from soot deposition or the introduction of foreign materials in the dermis after "cooking" of the drug and/or flaming of needles (Fig. 105-4).63
Track marks formed after repeated intravenous drug injections. (A) Inflammatory tracks of the dorsal hand, (B) inflammatory tracks with associated ulcers, nodules and abscesses on the hands and forearms, and (C) fibrotic tracks on the dorsal forearms.
"Soot tattoo." Soot tattoos result from the deposition of soot and other foreign materials in the dermis. Foreign materials may be introduced via adulterated drugs and/or introduction of needles with adherent soot after flaming for sterilization.
Diluting or "cutting" heroin to retail "street strength" is a common practice. Common diluents for white powder heroin include quinine, lactose, lidocaine, caffeine, lemon juice, inositol, dextrose, sucrose, procaine, starch, magnesium silicate and mannitol.64 Diluents may cause lymphatic destruction, foreign body granulomas, cutaneous nodules, ulcerations, panniculitis and dermal sclerosis secondary to irritation and dermal inflammatory processes (Fig. 105-5).65–67 The subsequent vascularized granulation tissue in and around chronic ulcers may be used as a site for drug injection.20 (see eFig. 105-5.1) Black tar heroin is a dark, gummy form of heroin that is less refined and cheaper than the white powder variant. It is mixed with a variety of diluents including dextrose, burnt cornstarch, instant coffee and dirt.68 The mixture may also contain dust and pathogens introduced during the process of manufacturing or storage.64,66 Irritant substances can also cause sterile chemical cellulites and abscesses.
Foreign body response and cellulitis. Angular ulcerations, firm erythematous nodules, and warm tender induration at the site of subcutaneous and intravenous injection of adulterated heroin.
Chronic ulcer at site of repeated cocaine injection. Repeated cocaine injection and subsequent chronic vasoconstriction at this site contributed to the formation and persistence of this significant ulcer. The highly vascularized overlying granulation tissue provides an excellent site for efficient injection drug use. The wound is dressed with Panafil® ointment, a compound containing papain, urea and chlorophyllin copper complex which was used at one time for its debriding properties.
Cutaneous infections are common in injection drug users (Table 105-1). Skin popping and black tar heroin use are associated with cutaneous necrosis and necrotizing ulcers.69–72 An increase in Clostridial infections including wound botulism due to Clostridium botulinum, tetanus due to Clostridium tetani, and rapidly progressive myonecrosis with a fulminant shock syndrome due to Clostridium sordellii have been observed with the use of black tar heroin in California.73–76
Fungi have been cultured from confiscated heroin specimens.77 Systemic candidosis characterized by painful nodules and pustules on the scalp and hair-bearing areas, chorioretinitis or uveitis, and costochondritis has been described in individuals injecting brown heroin diluted with lemon juice.78
Inhaling smoke and then exhaling it into another individual's mouth (known as shotgunning) is associated with efficient transmission of respiratory pathogens. 79
Opiates induce histamine release that results in subsequent pruritus that starts almost immediately after heroin injection and can last 10 minutes to 24 hours.80 Urticaria, severe angioedema and bronchospasm have also been reported with heroin use.80
Rare morbilliform eruptions, fixed drug eruptions and a case of toxic epidermal necrolysis have also been reported.62,64,81 Adulterants are thought to be responsible for most of these reactions.
Secondary systemic amyloidosis is an important cause of renal disease in heroin users. Its pathogenesis is thought to be associated with chronic antigenic stimulation and prolonged inflammation secondary to cutaneous infections. Patients were observed to progress to end stage renal disease over several months to 3 years.82
3,4-methylenedioxymethamphetamine (MDMA, ecstasy), along with lysergic acid diethylamide (LSD) and hallucinogenic mushrooms, is one of the most commonly used illicit hallucinogens (Table 105-1). More than 7 million persons have tried MDMA at least once in their lifetime. MDMA is a synthetic stimulant with psychoactive properties that acts both by causing a massive synaptic release of serotonin, and to a lesser extent dopamine and norepinephrine, as well as inhibiting the reuptake transporters within the synapse. Its short-term effects include inducing euphoria, a sense of enhanced intimacy with others, and diminished anxiety and depression. Adverse health effects can include nausea, chills, sweating, teeth clenching, muscle cramping, and blurred vision. MDMA is usually ingested, but may be injected or inhaled with effects lasting for 3–6 hours. It is frequently used in combination with alcohol, cannabis, amphetamine or cocaine, resulting in unpredictable effects.83
MDMA is associated with xerostomia and is therefore often coupled with soft drinks, which may lead to dental caries. The neurotransmitter release associated with MDMA induces bruxism, trismus and teeth grinding that can wear down tooth enamel. Direct application of MDMA to the gums may cause necrotizing gingivitis and widespread perioral and intraoral swelling. MDMA can also interfere with systemic temperature regulation that can, rarely, be lethal.
Methamphetamine is a very addictive synthetic stimulant that affects the brain and central nervous system through the release of dopamine, norepinephrine, and serotonin. By concurrently blocking reuptake of these neurotransmitters, sensations of euphoria, lowered inhibitions, feelings of invincibility, and hyperactivity are produced.84 Metamphetamine a white, odorless, bitter-tasting powder that can be ingested orally, snorted or injected. It may also be smoked in its rock "crystal" form.85 Short-term effects include feelings of euphoria, decreased fatigue associated with difficult life situations, headache, difficulty concentrating, diminished appetite, abdominal pain, vomiting, diarrhea, disordered sleep, paranoid or aggressive behavior, and psychosis. Long-term use of methamphetamine use is associated with anorexia, neurotoxicity, neurodegeneration, and clinical depression that may lead to homicidal and suicidal ideation and action.85
An increased rate of skin and soft tissue infections have been reported in methamphetamine users, including increased rates of methicillin-resistant Staphylococcus aureus (MRSA) infections in noninjection drug users. Methamphetamine use is associated with formication that can lead to subsequent skin picking, skin breakdown, and portals of infection (see eFig. 105-5.2). Use of methamphetamine and other sexually stimulating drugs can also increase direct skin-to-skin sexual contact and transmission of MRSA86 (Table 105-1).
Scars in a methamphetamine user. Angular atrophic white scars from skin-picking and excoriations in a former methamphetamine user. Methamphetamine commonly causes formication.
Methamphetamine users are at risk for developing meth mouth, or oral decay characterized by poor oral hygiene, xerostomia and rampant caries typically on the smooth surfaces of teeth, and excessive tooth wear.87 Methamphetamine use has also been associated with psychosis and subsequent self-injurious behavior including genital mutilation.88
Sedatives as a class of drugs includes benzodiazepines, hydroxybutyrate, flunitrazepam and cannabis. Cutaneous manifestations and reactions to this group of drugs is quite rare, however drug reactions have been rarely associated with benzodiazepines, including type IV morbilliform drug hypersensitivity eruptions,89 acute generalized exanthematous pustulosis to tetrazepam90 and erythema multiforme to clonazepam.91
Most anabolic steroids are synthetic substances similar to the male sex hormone testosterone. They may be ingested or injected, and are used especially by athletes to build muscle and enhance athletic performance. In 2000, approximately 3.6% of male and 0.9% of female twelfth graders in the United States had used anabolic steroids. Their abuse is most commonly associated with acne vulgaris, striae formation and alterations in hair growth.
Anabolic steroids induce sebaceous gland enlargement and the development of comedones through abnormal follicular keratinization.92,93 Steroid-associated acne is characteristically distributed on the face, shoulders, chest and back.93 It can progress to acne conglobata and fulminans secondary to the brisk immune response to Propionibacterium acnes in individuals who have never even had acne.94 Steroid-associated acne does not always respond to routine therapy and may persist for weeks to months following discontinuation of the drugs (see Chapter 80).93,95
Anabolic steroid use is also associated with alterations in hair growth, including hirsutism and androgenic alopecia, both of which are often more noticeable in women and may not be reversible with discontinuation of the drug.93,96,97 Males can develop testicular atrophy, gynecomastia and infertility. Women may experience menstrual changes, male-pattern alopecia, and deepening of the voice. Teenagers risk permanently stunted height and accelerated pubertal changes.
Steroid use is associated with striae formation secondary to dramatic hypertrophy of muscle tissue.98 Gingival enlargement has also been observed in those using anabolic steroids for greater than one year. Systemic effects of steroid abuse include hepatic damage, jaundice, hypertension and dyslipidemia.
Bacterial abscesses may occur at steroid injection sites secondary to nonsterile injection techniques.93,96 Repeated injection into the same site can result in inflammation and oil-induced granuloma formation.99 Soft tissue pseudotumors100 and rhabdomyolysis101 have also been reported in injectors.
In addition to causing de novo conditions, anabolic steroid use is also associated with exacerbation of existing acne and psoriasis.93 Case reports have described exacerbation of angiolipomas102 and latent acute hereditary coproporphyria as well.103
Through the use of tobacco, nicotine is one of the most heavily used addictive drugs in the United States. Cigarette smoking accounts for 90% of lung cancer cases in the US. Tobacco is an agricultural product processed from the leaves of plants in the genus Nicotiana, which can be smoked or chewed (more precisely, placed between gingival and buccal mucosa) to allow nicotine absorption via oral mucosa. Nicotine in the tobacco leaves is responsible for the vasoconstrictive effects of smoking via increased vasopressin secretion and stimulation of the sympathetic nervous system, thereby causing peripheral vasoconstriction.104–108 Smoking a single cigarette can produce cutaneous vasoconstriction for up to 90 minutes.109 Smoking decreases tissue oxygenation via vasoconstriction and by increasing carboxyhemoglobin, thereby limiting the blood's oxygen carrying capacity.110 Smoking also increases platelet aggregation111 and blood viscosity,112 and decreases prostacyclin formation.113 This combination of mechanisms also leads to impaired postoperative wound healing in smokers.114,115 The tar in cigarettes increases a smoker's risk of lung cancer, emphysema, and bronchial disorders. The carbon monoxide in smoke increases the chance of cardiovascular diseases.
Although the mechanism is unknown, smoking tobacco has also been linked with premature aging and rhytid formation. Elastin from photoprotecting skin in smokers is thick and fragmented, resembling that of sun-damaged skin but involving the reticular rather than the papillary dermis. Chronic dermal ischemia of as well as the decreased collagen synthesis likely play roles in the damaging elastic fibers.116 Increased plasma neutrophil elastase activity secondary to smoking may contribute to abnormal elastin.117 Smoking also causes a yellow–brown discoloration of the fingers and fingernails of digits habitually holding the cigarette (Fig. 105-6).118
The "nicotine sign." The orange hue of tobacco can lead to yellow–orange discoloration of the fingertips and fingernails in chronic cigarette smokers. Clubbing of the distal digits indicates the presence of chronic lung disease.
Cigarette smoking and chewing tobacco use are associated with a number of mucosal conditions. Leukokeratosis nicotinica palati (nicotine stomatitis, smoker's palate) is characterized by uniform keratosis of the hard palate with multiple tiny umbilicated erythematous papules representing the inflamed orifices of minor salivary glands.119 This benign oral lesion is seen exclusively in smokers and is caused by the tars and heat in tobacco smoke. Resolution is usually complete within 2 weeks of smoking cessation. All forms of tobacco use play a significant causative role in the development of leukoplakia.120 Leukokeratosis nicotinica glossae (also known as tongue) is a homogeneous leukoplakia affecting the anterior two-thirds of the dorsal tongue.121 Acute necrotizing ulcerative gingivitis "trench mouth," Vincent disease is caused by bacteria but is not communicable. Smokers tend to have fewer oral aphthous ulcers than nonsmokers due to decreased mucosal blood flow resulting from the vasoconstrictive effect of nicotine. Yellow discoloration of teeth secondary to tar deposition is also commonly observed.
Oral verrucous carcinoma, black hairy tongue, oral melanosis and oral warty dyskeratoma have been linked to tobacco use, but the connection is not as strong as in the aforementioned conditions.122,123
All forms of tobacco are associated with an increased risk of oral cancer.124–127 Cigarette smoke may act as a direct carcinogen or via systemic absorption.128,129 Smokers are also at an increased risk of developing squamous cell carcinomas at sites other than the oral mucosa, likely because of the immunosuppressive effects of smoking.130–132 Immune dysregulation associated with smoking is thought to be the reason that smokers with melanomas present with more advanced lesions and have a poorer disease prognosis.133,134
Thromboangiitis obliterans (Buerger disease) is an obstructive vascular disease that is indisputably associated with heavy cigarette smoking in young men. Cutaneous manifestations include blanching, cyanosis, burning, tingling, ulceration, necrosis, and gangrene (see Chapter 170).
Cigarette smoking has been shown to exacerbate and possibly induce palmoplantar pustulosis.135,136
Both allergic and irritant contact dermatitis characterized by itching and burning, have been documented to nicotine patches.137 Allergic contact dermatitis to the tobacco leaf has also been reported in tobacco harvesters and factory workers.138,139
Betel (Piper betle) belongs to the Piperaceae family; its leaf has an important social and cultural role in South Asia, Southeast Asia and the South Pacific. Betel leaves are chewed with the areca nut (also known as betel nut), calcium hydroxide, Acacia catechu bark, and occasionally tobacco in a wrapped package known as "betel quid." Betel leaves are used as a stimulant, antiseptic and breath freshener. The areca nut contains the alkaloid and stimulant arecoline which promotes salivation and stains saliva and teeth dark red to rust-colored. Calcium hydroxide keeps the active ingredients alkaline, thereby enabling its sublingual absorption and entry into the bloodstream.
Continuous chewing of betel quid maintains constant moisture at the oral commissures which, when coupled with continuous friction of opposing surfaces, causes maceration, erosion and fissures. These lesions can be mistaken for angular cheilitis, candidiasis or vitamin-deficiency associated perleche.140 The mixture is usually kept between the teeth and lip and may thus cause burning and erosions of the buccal mucosa.140 Chewer's mucosa results from the direct chemical action of the quid and/or traumatic effect of chewing, and is characterized by a brownish–red discoloration of the buccal mucosa with an irregular desquamative epithelial surface. These mucous membrane findings are not thought to be malignant or premalignant.141 Oral lichenoid lesions regress with decrease in frequency, duration or change in site of placement of the quid.142
Oral submucous fibrosis is directly related to betel quid chewing and affects the buccal mucosa, lips, retromolar areas, soft palate and occasionally the pharynx and esophagus.143 It is characterized by prodromal oral dysesthesia aggravated by spicy foods, followed by early blanching mottled mucosal lesions and subsequent late development of palpable vertical fibrous bands in the buccal mucosa and around the mouth opening requiring surgical release for sufficient opening of the mouth.144 Trismus, dysphagia, xerostomia, rhinolalia and tongue stiffening present late in the disease course. Mucosal petechiae, leukoplakia and epithelial dysplasia are also seen.145,146 The most serious complication of oral submucous fibrosis is the development of oral carcinoma, which can be seen in up to 10% of users and is typically localized to the buccal tongue and labial mucosa.147 Of all oral cancers in Taiwan, as many as 86.2% of cases have been reported to be in betel quid chewers.148
Polysubstance Abuse
Polysubstance abuse, the concurrent use of several drugs with different pharmacologic effects, is becoming increasingly common. The diversity of reported drug use combinations suggests that achieving some perceptible change in state may be the primary motivator driving this practice. One drug may be used to enhance the effects of another, as with the combined use of benzodiazepines and methadone or cocaine and heroin (speedballs). Polysubstance abuse can cause adverse health consequences, such as pulmonary disease, reproductive dysfunction and immunosuppression in chronic cocaine and psychostimulant abuse. It may also exacerbate preexisting conditions such as hypertension and cardiac disease. The concurrent use of some drugs, including cocaine and opiates, is frequently associated with deleterious behavior such as needle sharing by injection drug users.
In addition to the local reactions and systemic effects of specific drugs themselves complications of drug use must also be considered.
Injection drug use is associated with inoculation and transmission of infectious agents leading to local skin and soft tissue infections and abscesses, as well as the subsequent hematogenous spread of microbes. Gram-positive cocci including Staphylococcus aureus, group A β-hemolytic streptococcus and other streptococci are the most commonly observed microbial agents.149–151 Anaerobes are the second most common group of bacteria to be isolated, while Gram-negative bacteria are less commonly isolated. The source of the pathogens is variable, but most originate from the flora of the skin and oropharynx secondary to needle-licking practices and use of saliva to clean or moisten skin and injection implements.149 Abscesses and cellulitis occur in 22%–65% of drug users152 (Fig. 105-7). Irritant substances including the drug or its diluents may cause sterile chemical cellulitis and abscesses. Systemic infections including bacteremia, endocarditis, osteoarthritis, and systemic candidosis may result. Systemic candidosis is the most common systemic fungal infection in injection drug users (Table 105-2).
Cellulitis at the site of repeated drug injection. Tender warm erythema and induration surrounding a chronic ulceration at the site of routine drug injection. Secondary infections at injection sites can be caused by introduction of pathogens via unsterilized needles, adulterated drugs, and at sites of compromised skin integrity. S. aureus infectious endocarditis occurred following bacteremia from this site.
Table 105-2 Common Infectious Agents Associated with Drug Abuse and Addiction
Infectious Agent
Streptococcal species
Anaerobes
Unusual organisms
Aspergillus
Mucor
herpatic viruses
Human T-cell lymphotropic virus
Hepatitis B virus
Sexually transmitted
Human papilloma viruses
Treponema pallidum
Direct intra-arterial injection of drugs may cause severe ischemia and necrosis. Early intense burning is noted in the injected area, followed by marked edema, compartment syndrome, cyanosis, and livedoid patches of the affected limb within a few hours. Distal necrosis may occur in the most severe cases, and has been seen with the use of drugs such as cocaine, heroin, pentazocine, diazepam, amphetamine and others25,153,154 The local cytotoxicity of a drug may cause a chemical endarteritis resulting in vasospasm and thrombosis.
The behavioral effects of injection drug use has been associated with an increased risk of sexually transmitted diseases as well as blood-borne diseases transmitted through unsterilized needles including hepatitis B virus (HBV), hepatitis C virus (HCV), human immunodeficiency virus (HIV) and human T-lymphotropic virus (HTLV) (Table 105-2).
The repeated trauma of venipuncture, local infections and the irritant drugs and adulterants can lead to superficial and deep venous thrombosis. Chronic venous insufficiency can result from vein trauma, necrotic ulcers at sites of past subcutaneous injection, vein thrombosis and blockage of the lymphatic system.155,156
Other noninfectious diseases associated with drug use include psychiatric disease, accidental injury due to altered mental status and trauma due to criminal violence or domestic abuse.
While mucocutaneous findings can be suggestive of drug use drug testing is needed to identify the agents used. Bodily fluids including saliva, blood, urine and hair can be used in drug detection. Urinalysis for qualitative detection of psychoactive substances and their metabolites is often the fastest way to determine ingestion of a substance (Table 105-3).
Table 105-3 Drug Detection in Body Fluids and Hair
Blood/Saliva
Up to 90 days
Amphetamines (except meth)
MDMA (Ecstasy)
Therapeutic use: 0–7 days Chronic use (>1 year) 4–6 weeks
2–3 days, up to 2 weeks in heavy users
3–7 days, up to >30 days after heavy use and/or in users with high body fat
2–5 days with exceptions for certain kidney disorders
Cotinine (break-down product of nicotine)
24–72 hours (tests for LSD are very uncommon)
3–7 days for single use; up to 30 days in chronic users
Urine data from Labcorp I. Drugs of Abuse Reference Guide, 2004, https://www.labcorp.com/pdf/doa_reference_guide.pdf. accessed May 1, 2011.
Systemic conditions secondary to the effects of substance abuse should also be part of the evaluation of these patients. Cutaneous infections at sites of trauma, ulcers, or necrosis should be swabbed or biopsied for culture to identify and treat causative organisms. Thorough evaluation and imaging may be required to rule out injury to or involvement of vital organs and bony structures. In injection drug users, thorough cardiac evaluation and examination of mucocutaneous and acral surfaces should be undertaken to access for embolic phenomenon. Evaluation for transmitted infections such as HIV, hepatitis and sexually transmitted diseases may be required.
It is imperative to rule out primary infectious causes of ulcers, nodules, skin and subcutaneous infections in suspected drug users. Inflammatory and vasculopathic processes such as pyoderma gangrenosum, livedoid vasculopathy and medium vessel vasculitides must be considered in the setting of ulcers and nodules. Evidence of distal vascular compromise can be seen in pernio, thromboembolic phenomenon and Raynaud phenomenon. The edematous phase of scleroderma, eosinophilic fasciitis and secondary lymphatic obstruction are rare entities to consider the setting of distal extremity swelling. Infectious and noninfectious granulomatous diseases [including tuberculosis, leishmaniasis, granulomatosis with polyangiitis (Wegener's) and sarcoidosis] can present with nasopalatal infiltration and perforation. Patients with pruritus and formication may require evaluation for infestation, metabolic or psychiatric etiologies of their symptoms.
A detailed discussion of the treatment of drug abuse and dependence is beyond the scope of this chapter, but it is essential to recognize that these are chronic illnesses that require long-term strategies. Combined medical and behavioral therapy are important elements of a therapeutic process comprising detoxification, treatment and relapse prevention. Amelioration of withdrawal symptoms is key to initiation of therapy. A multidisciplinary approach including addiction counseling, social work support and management of associated infectious, vascular, cardiac and hepatic complications is critical to comprehensive care.
Potential therapies for opiate dependence include drug detoxification (office-based, inpatient or ultra rapid under anesthesia), agonist maintenance (injectable diacetylmorphine, methadone, levomethadyl or buprenorphine), antagonist maintenance (naltrexone)and pharmacologic treatment of withdrawal symptoms (clonidine, lofexidine or guanfacine).
Treatment options for tobacco addiction include nicotine replacement therapies (patch, spray, gum and lozenges). Bupropion and varenicline have been approved by the Food and Drug Administration for management of nicotine addiction. Behavioral interventions include group and individual therapies, and telephone quitlines.
Outpatient and residential treatment centers can provide environments in which individuals can participate in therapeutic communities and benefit from behavioral therapy and peer support. Alternative therapies including acupuncture may also prove useful in combination with medical and behavioral therapeutic interventions. Although relapses are common, successful outcomes are accomplishable, indicating the importance of candid, supportive, nonjudgmental, care-facilitating discussions in patients whose drug use has been revealed through skin examination.
The transmission of infectious disease via injection drug use can be addressed by encouraging physicians to prescribe sterile injection equipment, setting up injection rooms staffed by healthcare personnel who can provide advice on safe injection techniques and instituting strictly supervised heroin, diamorphine or buprenorphine prescription programs for long-term injectors.157 This may help reduce the risk of life-threatening infection from nonsterilized drugs, prevent overdose from drugs of unknown purity, break the link between drug use and criminal activity to acquire drugs and decrease the number of injections in public places.
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Being in Mölle to attend the 17th annual conference on European Integration in Swedish Economic Research, SNEE 2015, provided the opportunity to visit Kullen Lighthouse or Kullens fyr in the neighbouring town of Höganäs.
The lighthouse serves as a steering marker for one of the world's most traveled waters.
A prominent landmark along the Swedish southwest coast, Kullen Lighthouse, with its 1000 Watt electric bulb encased in a large lenshouse is the strongest operational lighthouse in Scandinavia situated at the mouth of Öresund, at the tip of Kullaberg peninsula in Höganäs. It overlooks one of the world's most heavily traveled waters.
The lighthouse is nestled atop Kullenberg Nature Reserve that houses some exotic and rare species of plants that grow favourably in the Scandinavian climate including birch, juniper, hawthorne and honeysuckle. Visitors to this nature reserve can get there by hiking from the harbour town of Mölle that depending on your own boarding arrangements could take about an hour and a half. One could also drive, or go with a chartered tour bus.
An old apple tree that is seeing the benefits of non-pruning.
Just across from the windmill set against dramatic dark clouds, a more than sun-drenched field of flowers.


Update your formal attire with this men's shirt from the Armani Collezioni collection. This navy blue shirt features a micro diamond textured pattern throughout and a slight sheen. Details: full button placket, button cuffs, long sleeves, tonal stitching throughout and a regular fit. Our model is 6'1" with a 38" chest and wears a medium.


Enjoy the holiday sounds of the George Fremont Trio!! They will be back in to perform some of your favorite holiday tunes for you as you sip on wine, relaxing the day away! Unwind from your shopping and enjoy your time with us.
Also enjoy chocolates from local favorite Wellington Chocolates.


When Donald Trump won the presidential vote last year there was an outcry from his opponents due to his alleged close ties with the Russian government. Many believed that Trump would be quick to remove U.S. economic sanctions against Russia, thus stimulating economic growth in the country and making it more daring territorially.
This has not happened and is unlikely to happen, as is becoming increasingly obvious. The sanctions have remained, and so have low oil prices, pressuring Russia's growth and stock market. These two factors are seen by some analysts as the drivers behind equity price trends in the country.
According to CNBC, the Moscow Composite Index, or Micex, is down 8 percent in the past three months, underperforming the U.S. stock market by 15 percent, thanks to Trump's vow to keep sanctions in place and, of course, the new lower normal for oil prices.
Now, investors are naturally wary of tapping a market that is the object of economic sanctions, even though the last two months of 2016 saw a 15 percent jump in Micex, driven by expectations of a warming in bilateral relations. This decline in equity prices we are witnessing now was to be expected once it became clear that this warming – if it takes place at all – will not be a quick deal.
In terms of relative weight, however, oil prices may have more to do with stock market developments in the world's largest oil exporter. Despite much praise for OPEC's deal, which saw the cartel and 11 other producers pledge to remove some 1.8 million barrels of crude from the global market, it has so far failed to bring prices much higher.
This is concerning for Saudi Arabia and other Gulf producers, as it surfaced recently, but it does not seem to be bothering the Kremlin. At the start of this year, Deputy Finance Minister Anton Siluanov said that the country could return to positive GPD growth in three years if Brent remains at US$50 a barrel. Each additional US$10 per barrel translates into over US$28 billion in state revenue.
Analysts believe that the downward trend in the Micex will continue through the rest of the year. This is, again, only to be expected – quick spikes in equity markets driven by a single event and its potential implications are often short-lived, just like the jumps in oil prices that followed every statement from an OPEC or Russian oil official in the months leading up to the November 30 production cut deal.
Chances are, however, that the drop will slow down, unless the new administration changes its stance on Russia to an openly hostile one. Let's not forget, after all, that the U.S. sanctions against Russia are not of the blanket type: they target specific individuals and legal entities close to President Vladimir Putin. This curbs the adverse effects in the context of equity market trends, so some investors can still do business in Russia.
Oil prices are likely to remain around the US$55 a barrel mark for Brent and a little lower for WTI. Sanctions are also likely to remain in place. This means that Russian stocks are likely to continue their slide, but the slide will probably slow as the Trump hype fades and Russian stock markets return to business as usual.